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immunosuppressants Flashcards

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1
Q

rheumatoid arthritis pathophysiology

A

Inflammatory change and proliferation of synovium
leading to dissolution of cartilage and bone
can lead to erosion of the joint
more expression of pro inflammatory cytokines (IL1,IL6, TNFalpha)
antibodies produced by B cells: Rheumatoid factor, Anti-CCP antibodies

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2
Q

clinical criteria for Ra

A

• Morning stiffness more than 1 hour • Arthritis of more than 3 joints • Arthritis of hand joints • Symmetrical arthritis • Rheumatoid nodules

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3
Q

non-clinical criteria for RA

A

• Serum rheumatoid factor/Anti-CCP antibodies • X-ray changes

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4
Q

treatment goals

A

 Symptomatic relief  Prevention of joint destruction

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5
Q

treatment strategies for Ra

A 
• Early use of disease-modifying drugs 
• Aim to achieve good disease control 
• Use of adequate dosages 
• Use of combinations of drugs
 • Avoidance of long-term corticosteroids
drug induced remission
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6
Q

Treatment goals in SLE & vasculitis

A
  • Symptomatic relief e.g arthralgia, Raynaud’s phenomenon
  • Reduction in mortality
  • Prevention of organ damage
  • Reduction in long term morbidity caused by disease and by drugs
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7
Q

corticosteroids mechanism

A

Upregulate anti-inflammatory and downregulate pro-inflammatory genes

(• Prevent interleukin IL-1 and IL-6 production by macrophages • Inhibit all stages of T-cell activation)

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8
Q

corticosteroid examples

A 
Non-biologics 
• Sulphasalazine gut and joint
• Hydroxychloroquine lupus, immuno modulatory effect
Biologics 
• Anti-TNF agents 
• Rituximab 
• IL-6 inhibitors, JAK inhibitors
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9
Q

Azathioprine indication

A

• SLE & vasculitis -as maintenance therapy
steroid sparing drug
atopic dermatitis, bulbous skin disease

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10
Q

Azathioprine mechanism

A

• metabolized by TPMT
• TPMT gene highly polymorphic Low/absent TPMT levels = Risk of
myelosupression • Therefore test TPMT activity before prescribing

Inhibits synthesis of purines needed for DNA and RNA replication

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11
Q 
#Azathioprine
(All immunosuppressants)
A 
• Bone marrow suppression
– Monitor FBC 
• Increased risk of malignancy
• Increased risk of infection 
• Hepatitis – Monitor LFT

Other immunosuppressants -caution

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12
Q

Calcineurin inhibitor examples

A

Ciclosporin & tacrolimus

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13
Q

Calcineurin inhibitor indication

A

transplantation, atopic dermatitis, psoriasis

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14
Q

Calcineurin inhibitor

A

renal toxicity, gum hypertrophy

check BP, eGRF regularly

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15
Q

^ Calcineurin inhibitor

A

CYP 450 drugs inducers and inhibitors

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16
Q

Calcineurin inhibitor mechanism

A

Active against helper T-cells, preventing production of IL-2 via calcineurin inhibition

reduce helper T-cell activity

17
Q

Mycophenolate mofetil indication

A

transplantation
induction, maintenance of lupus nephritis
maintenance of vasculitis

18
Q

Mycophenolate mofetil mechanism of action

A
  • impairs B- and T-cell proliferation

* spares other rapidly dividing cells (due to guanosine salvage pathways in other cells)

19
Q

Mycophenolate mofetil

A

• Most common include nausea, vomiting, diarrhea
• Most serious is myelosuppression
caution with vaccinations

20
Q

Cyclophosphamide indication

A

– Lymphoma, leukaemia, solid cancers
– Lupus nephritis
– Wegener’s granulomatosis (ANCA-vasculitis)

caution with vaccinations

21
Q

Cyclophosphamide action

A

Alkylating agent -cross links DNA so that it cannot replicate
– suppresses T and B cell activity
prodrug, converted in liver by CYP450, excreted by kidney.
metabolites:toxic to the bladder epithelium and can lead to hemorrhagic cystitis
• This can be prevented through the use of aggressive hydration and/or Mesna)

22
Q

cyclophosphamide

A 
• Significant toxicity
– increased risk of bladder cancer, 
– Infertility
– monitor FBC
– Adjust dose in renal impairment
 max 30g in a lifetime
23
Q

methotrexate indication

A

RA,
malignancy, psoriasis, Crohn’s disease
Unlicensed roles: Inflammatory
myopathies,vasculitis, steroid-sparing agent in asthma

24
Q

methotrexate mechanism of action

A

• Mechanism of action in non-malignant disease e.g. RA, psoriasis is NOT CLEAR
• Mechanism is not via anti-folate action
Inhibition of accumulation of adenosine
– the inhibition of T cell activation
– suppression of intercellular adhesion molecule expression by T cells

Malignant:
inhibits the synthesis of DNA, RNA and proteins
hence cytotoxic

25
Q

methotrexate pharmacokinetics

A

• WEEKLY NOT DAILY DOSING ,bioavailability increases S/C,
50% protein bound-
NSAIDs drug-drug interaction,
renal excretion

26
Q

methotrexate

A 
• mucositis 
• marrow suppression both respond to folic acid supplementation
• Highly teratogenic, abortifacient
Rare:
• hepatitis, cirrhosis, • pneumonitis 
• infection risk
27
Q

sulfasalazine mechanism

A 
disease modification • T-cell
– inhibition of proliferation
– possible T-cell apoptosis
– inhibition of IL-2 production 
• Neutrophil
– reduced chemotaxis and degranulation
poorly absorbed- active in intestine effective in IBD

Release 5-aminosalicylic acid (5-ASA) - immunosuppressive

28
Q

sulfasalazine

A 
• Mainly due to sulfapyridine moiety
– myelosuppression
– hepatitis
– Rash
• Milder side effects
– nausea
– abdo pain/vomiting
safe in pregnancy
, hypersensitivity
29
Q

anti TNF alpha mechanism

A

reduce Inflammation
reduce Cytokine cascade
reduced Recruitment of leukocytes to joint
elaboration of adhesion molecules production of chemokines
reduced Angiogenesis
reduced Joint destruction, Bone resorption and erosion, Cartilage breakdown

30
Q

TB and TNF

A

TNFα is essential for development + maintenance of granulomata
Screen for latent TB before anti-TNF treatment
TNFα is released by macrophages in
response to M TB infection

31
Q

rituximab mechanism

A

causes B cell apoptosis

Very effective in RA.

32
Q

corticosteroid

A

Immunosuppression, adrenal insufficiency,

33
Q

^ corticosteroids

A

Affected by CYP inducers,
bleeding risk increased with NSAIDs,
insulin

CPT (19 decks)

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